ArticleNature communications2025
Astrocytic pleiotrophin deficiency in the prefrontal cortex contributes to stress-induced depressive-like responses in male mice.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Rosiglitazone Adjunct to Sertraline for Major Depressive Disorder: A Randomized, Double-Blind, Placebo-Controlled Trial.Depression and anxiety · 2026Trial
- MFN2-associated astrocyte dysfunction contributes to neuronal hyperexcitability and depressive-like behaviors.Science advances · 2026Article
- Astrocyte reactivity by alcohol dependence in the central amygdala.Brain, behavior, and immunity · 2026Article
- Impaired Brain Astrocytic Glycolysis in Neuropathic Pain: Insights from Transcriptomic Profiling to Metabolic Intervention.International journal of molecular sciences · 2026Article
- Chronic stress activates a hypothalamic vagal circuit to promote hepatocellular carcinoma progression in male mice.Nature communications · 2026Article
- Disrupted TFEB/GDNF-cAMP/ATP Coupling Underlies Astrocytic Dysfunction and Depression in LRRK2 G2019S Parkinson's Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Antidepressant Effects of 20-Glucoginsenoside Rf in an L-AAA-Induced Mouse Model with Glial-Associated Molecular Alterations.Current issues in molecular biology · 2026Article
- The Gut Microbiota-Astrocyte Axis: New Insights into the Mechanisms of Comorbid Major Depressive Disorder in Type 2 Diabetes Mellitus.Molecular neurobiology · 2026Review
- Article
- AiScience · 2026Article
- Molecular and Cellular Mechanisms Linking Mood Disorders, HPA Axis Dysregulation, and Neurocognitive Inflammation to Perioperative Neurocognitive Disorders.Biomolecules · 2026Review
- Pleiotrophin regulates presynaptic assembly and function through heparan sulfate-dependent binding to neurexin1.Cell reports · 2026Article
- FGF13 alleviates astrocytic apoptosis via JIP2 inhibition in the hippocampus and mitigates depression-like behavior.Journal of neuroinflammation · 2026Article
- AI-driven tripartite classification for optimizing wearable bioelectronics in depression management.Science advances · 2026Article
- Article
- Astrocyte Reactivity by Alcohol Dependence in the Central Amygdala.bioRxiv : the preprint server for biology · 2026Article
- Reprogramming of neuronal genome function and phenotype by astrocytes.bioRxiv : the preprint server for biology · 2026Article
- Single-nucleus RNA sequencing and functional studies of acute methamphetamine-induced cognitive impairment.Communications biology · 2026Article
- From metabolism to mood regulation: astrocytes as a driver of depression.Frontiers in cellular neuroscience · 2026Review
- Integrative multi-omics and machine learning analysis identifies candidate biomarkers associated with mitochondrial quality control in major depressive disorder.Frontiers in psychiatry · 2026Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Astrocytes are closely linked to depression, and the prefrontal cortex (PFC) is an important brain region involved in major depressive disorder (MDD). However, the underlying mechanism by which astrocytes within PFC contribute to MDD remains unclear. Using single-nucleus RNA sequencing analyses, we show a significant reduction in astrocytes and attenuated pleiotrophin-protein tyrosine phosphatase receptor type Z1 (PTN-PTPRZ1) signaling in astrocyte-to-excitatory neuron communication in the PFC of male MDD patients. We find reduced astrocytes and PTN in the dorsomedial PFC of male mice with depression induced by chronic restraint and social defeat stress. Knockdown of astrocytic PTN induces depression-related responses, which is reversed by exogenous PTN supplementation or overexpression of astrocytic PTN. The antidepressant effects exerted by astrocytic PTN require interaction with PTPRZ1 in excitatory neurons, and PTN-PTPRZ1 activates the AKT signaling pathway to regulate depression-related responses. Our findings indicate the PTN-PTPRZ1-AKT pathway may be a potential therapeutic target for MDD.
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